The object of this study is to clarify the relationsip between oxygen tension, metabolic activty and atheromatosis in the arterial wall. While most reports agree that artery metabolism undergoes some change before as well as during atherogenesis, there is no unanimity as to the role of PO2 and whether QO2 increases or decreases. Knowledge of the changes in energy pattern during atherogenesis should help our understanding of the mechanisms involved in the initiation of plaques and in their subseqent progressson. Part of the confusion in the O2-atherosclerosis relationship may be the result of a lack of specificity in way the comparisons are carried out; this is usually between an overall O2 uptake measurement for an entire segment of artery and an overall sbjective score for the range of disease normally present in that segment. Considering the focal nature of atherosclerosis and its tendency to localize in the intima, we propose that a more meaningful analysis would result from a point-by-point comparison between the oxygen measurements and lesion severity over the endothelial surface of the affected vessel. The recent availability of micro-O2 electrodes makes such an undertaaing experimentally feasable with respect to PO2. To help the result of a point-by-point mapping of the intima into perspective, the study would include the more conventional measurements of average metabolic activity, average atherosclerotic involvement and average chemical composition of the respective arterial segments. Comparisons between PO2 and QO2 will further aid in estimmting O2 diffusion limitations.